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Upper Gastrointestinal Bleeding

  • Author: Maurice A Cerulli, MD, FACP, FACG, FASGE, AGAF; Chief Editor: BS Anand, MD  more...
 
Updated: Mar 21, 2016
 

Practice Essentials

Acute gastrointestinal bleeding is a potentially life-threatening abdominal emergency that remains a common cause of hospitalization. Upper gastrointestinal bleeding (UGIB) is defined as bleeding derived from a source proximal to the ligament of Treitz.

The image below depicts an ulcer with active bleeding.

Ulcer with active bleeding. Ulcer with active bleeding.

Signs and symptoms

Signs and symptoms of acute upper GI bleeding[1] include the following:

  • Hematemesis
  • Melena
  • Hematochezia
  • Syncope
  • Presyncope
  • Dyspepsia
  • Epigastric pain
  • Heartburn
  • Diffuse abdominal pain
  • Dysphagia
  • Weight loss
  • Jaundice

See Clinical Presentation for more detail.

Diagnosis

Workup includes the following:

  • Orthostatic blood pressure
  • Complete blood count with differential
  • Hemoglobin level
  • Type and crossmatch blood
  • Basic metabolic profile, blood urea nitrogen, and coagulation profile
  • Calcium level
  • Gastrin level
  • Endoscopy
  • Chest radiography
  • Nasogastric lavage
  • Angiography (if bleeding persists and endoscopy fails to identify a bleeding site)

Computed tomography scanning and ultrasonography may be indicated for the evaluation of the following[2] :

  • Liver disease with cirrhosis
  • Cholecystitis with hemorrhage
  • Pancreatitis with pseudocyst and hemorrhage
  • Aortoenteric fistula

See Workup for more detail.

Management

Treatment includes the following:

  • Secure the airway
  • Insert bilateral, 16-gauge (minimum), upper extremity, peripheral intravenous lines
  • Replace each milliliter of blood loss with 3 mL of crystalloid fluid
  • In patients with severe coexisting medical illnesses, pulmonary artery catheter insertion for monitoring hemodynamic cardiac performance
  • Foley catheter placement for continuous evaluation of urinary output as a guide to renal perfusion
  • Endoscopic hemostatic therapy for bleeding ulcers and varices
  • Surgical repair of perforated viscus
  • For high-risk peptic ulcer patients, high-dose intravenous proton pump inhibitors

Indications for surgery in patients with bleeding peptic ulcers include the following:

  • Severe, life-threatening hemorrhage not responsive to resuscitative efforts
  • Failure of medical therapy and endoscopic hemostasis with persistent recurrent bleeding
  • A coexisting reason for surgery (eg, perforation, obstruction, malignancy)
  • Prolonged bleeding, with loss of 50% or more of the patient's blood volume
  • A second hospitalization for peptic ulcer hemorrhage

See Treatment and Medication for more detail.

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Background

Acute gastrointestinal (GI) bleeding is a potentially life-threatening abdominal emergency that remains a common cause of hospitalization.[3, 4] Upper gastrointestinal bleeding (UGIB) is defined as bleeding derived from a source proximal to the ligament of Treitz.[5]

The incidence of UGIB is approximately 100 cases per 100,000 population per year.[6] Bleeding from the upper GI tract is approximately 4 times more common than bleeding from the lower GI tract and is a major cause of morbidity and mortality. Mortality rates from UGIB are 6-10% overall.[6] (See Epidemiology, below.)

The diagnosis of and therapy for nonvariceal upper gastrointestinal bleeding (UGIB) has evolved since the late 20th century from passive diagnostic esophagogastroduodenoscopy with medical therapy until surgical intervention was needed to active intervention with endoscopic techniques followed by angiographic and surgical approaches if endoscopic therapy fails.[7] (See Workup and Treatment and Management, below.)

Variceal hemorrhage is not discussed in this article because the underlying mechanisms of bleeding are different and require different therapies.

The underlying mechanisms of nonvariceal bleeding involve either arterial hemorrhage, such as in ulcer disease and mucosal deep tears, or low-pressure venous hemorrhage, as in telangiectasias and angioectasias. In variceal hemorrhage, the underlying pathophysiology is due to elevated portal pressure transmitted to esophageal and gastric varices and resulting in portal gastropathy. A bleeding ulcer is seen below. (See Etiology, below.)

Go to Pediatric Gastrointestinal Bleeding for complete information on this topic.

Ulcer with active bleeding. Ulcer with active bleeding.

In patients with UGIB, comorbid illness, rather than actual bleeding, is the major cause of death. Comorbid illness has been noted in 50.9% of patients, with similar occurrences in males (48.7%) and females (55.4%).

One or more comorbid illnesses have been noted in 98.3% of mortalities in UGIB; in 72.3% of patients, comorbid illnesses have been noted as the primary cause of death.[8, 9] (See Epidemiology and Prognosis, below.)

Significant comorbidities have become more prevalent as the patient population with UGIB has become progressively older. In a retrospective chart review by Yavorski et al, 73.2% of deaths occurred in patients older than 60 years.[9] (See Epidemiology and Prognosis, below.)

Rebleeding or continued bleeding is associated with increased mortality; therefore, differentiating the patient with a low probability of rebleeding and little comorbidity from the patient at high risk for rebleeding with serious comorbidities is imperative. (See Clinical Presentation and Workup, below.)

Peptic ulcer disease and UGIB

Peptic ulcer disease (PUD) remains the most common cause of UGIB. In a literature review involving more than 10,000 patients with UGIB, PUD was responsible for 27-40% of all bleeding episodes.[10] High-risk patient populations at risk for PUD include those with a history of alcohol abuse, chronic renal failure, and/or nonsteroidal anti-inflammatory drug (NSAID) use.[11]

Peptic ulcer disease is strongly associated with Helicobacter pylori infection. The organism causes disruption of the mucous barrier and has a direct inflammatory effect on gastric and duodenal mucosa, reducing mucosal defenses and increasing back diffusion of acid by loosening the tight cellular junctions. (Rates of H pylori infection are reportedly lower in patients with complicated ulcer disease than in patients with uncomplicated ulcers. Hosking et al reported a 71% incidence of H pylori infection in patients with bleeding duodenal ulcers; patients with nonbleeding ulcers had an incidence of 93%.) This discrepancy may be due to the decrease in sensitivity of biopsy in patients with ulcer bleeding.[12]

Eradication of H pylori been demonstrated to reduce the risk of recurrent ulcers and, thus, recurrent ulcer hemorrhage after the initial episode. In fact, the proportion of UGIB cases caused by peptic ulcer disease has declined,[13] a phenomenon that is believed to be due to the use of proton pump inhibitors (PPIs) and H pylori therapy.

Duodenal ulcers are more common than gastric ulcers, but the incidence of bleeding is identical for both. In most cases, the bleeding is caused by the erosion of an artery at the base of the ulcer. In approximately 80% of patients, bleeding from a peptic ulcer stops spontaneously.[10]

Initial endoscopic attempts to maintain hemostasis have a high failure rate. Bleeding vessels larger than 1.5 mm in diameter are associated with an increased mortality rate due to the difficulty in producing adequate hemostasis with thermal probes.

A minority of patients experience recurrent bleeding after endoscopic therapy, and these cases are usually associated with risk factors for rebleeding. These factors include age older than 60 years, the presence of shock upon admission, coagulopathy, active pulsatile bleeding, and the presence of cardiovascular disease. (The appearance of the ulcer at the time of endoscopy provides important information regarding the risk of rebleeding.) These circumstances are associated with a poorer prognosis and a higher mortality rate.[14]

Despite the dangers associated with a bleeding peptic ulcer, a study by Sung et al of 10,428 cases of such bleeding (in 9,375 patients) found that most deaths were not caused by it.[15] Of the 577 deaths that occurred in the cohort, almost 80% resulted from other causes, including multiorgan failure, pulmonary conditions, and terminal malignancy. The authors concluded that the management of patients with peptic ulcers should focus not only on hemostasis but also on lowering the risk of multiorgan failure and cardiopulmonary death.

Recurrent bleeding risk in peptic ulcers

Forrest et al were the first to classify the stigmata of hemorrhage from peptic ulcers. Based on these classifications, the risk of recurrent bleeding can be predicted. The ulcers at highest risk for rebleeding are those that involve active arterial bleeding or those with a visible, protuberant, nonbleeding vessel at the base of the ulcer. The study not only correlated the incidence of rebleeding with the stigmata of recent bleeding and the endoscopic appearance of an ulcer, but also determined prognostic information regarding the need for surgery. Mortality was also correlated with these factors.[16]

In patients with H pylori infection, the rate of recurrent bleeding is extremely low. This is why documenting the presence of H pylori and aggressively treating the infection are important.

Patients who are not infected with H pylori may require a subsequent acid-lowering surgical procedure or long-term medical therapy for recurrent ulcer disease and bleeding.

Other causes of UGIB

Other major causes of UGIB are mucosal tears of the esophagus or fundus (Mallory-Weiss tear), erosive gastritis, erosive esophagitis, Dieulafoy lesion, gastric cancer, and ulcerated gastric leiomyoma.

Patients with chronic liver disease and portal hypertension are at an increased risk for variceal hemorrhage and portal gastropathy in addition to ulcer hemorrhage.

Rare causes of UGIB include aortoenteric fistula, gastric antral vascular ectasia, angiectasias, and Osler-Weber-Rendu syndrome.

An aortoenteric fistula results from the erosion of the aortic graft into the bowel lumen, usually at the third or fourth portion of the duodenum. The result is a direct communication between the aortic graft lumen and the bowel lumen. Most aortoenteric fistulas involve the proximal aortic anastomotic suture line.

UGIB can also result from acute stress gastritis, a disease process characterized by diffuse superficial mucosal erosions that appear as discrete areas of erythema.[16] The bleeding is usually mild and self-limiting and rarely progresses to life-threatening hemorrhage.

In intensive care unit (ICU) patients, the incidence of clinically significant GI bleeding (eg, hypotension, transfusion) from acute stress gastritis was found to be 1.5%.[17] Stress gastritis and mucosal ulceration are historically associated with (1) head injuries with associated elevations in intracranial pressure and (2) burn injuries. These stress ulcers are called Cushing ulcers and Curling ulcers, respectively.

Angiodysplasia of the upper GI tract accounts for 2-4% of bleeding lesions.[10] The condition is also a cause of lower GI bleeding in 6% of cases.[16] The lesion is a vascular malformation that represents an abnormal dilation of mucosal and submucosal vessels.

Histologically, angiodysplasias are dilated, thin-walled vascular channels that appear macroscopically as a cluster of cherry spots. When located in the upper GI tract, they most commonly involve the stomach and duodenum. The lesions can be acquired or congenital, as in hereditary hemorrhagic telangiectasia and Rendu-Osler-Weber syndrome.

The acquired angiodysplasias are commonly found in patients with chronic renal failure requiring hemodialysis and with aortic valvular disease (especially aortic stenosis). Other diseases, such as cirrhosis and von Willebrand disease, are associated with a higher frequency of angiodysplasias. Most lesions are smaller than 1 cm in diameter and can be multiple in 66% of patients.[10]

For patient education information, see the Digestive Disorders Center and the Heartburn and GERD Center, as well as the patient education article Gastrointestinal Bleeding (GI Bleeding).

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Etiology

Ulcer-related UGIB

Bleeding peptic ulcers account for the majority of patients presenting with acute upper gastrointestinal bleeding (UGIB).[3]  As previously mentioned, peptic ulcer disease is strongly associated with H pylori infection. The organism causes disruption of the mucous barrier and has a direct inflammatory effect on gastric and duodenal mucosa.

In cases of ulcer-associated UGIB, as the ulcer burrows deeper into the gastroduodenal mucosa, the process causes weakening and necrosis of the arterial wall, leading to the development of a pseudoaneurysm. The weakened wall ruptures, producing hemorrhage.

The flow through a vessel varies with the fourth power of the radius; thus, small increases in vessel size can mean much larger amounts of blood flow and bleeding, with more severe hypotension and more complications, especially in older patients.

Visible vessels usually range from 0.3-1.8 mm.

Exsanguinating hemorrhage has been reported from larger vessels. The larger vessels are located deeper in the gastric and duodenal submucosa and serosa. Larger branches of the left gastric artery are found high on the lesser curvature, while the pancreatoduodenal artery and its major branches are located posteroinferiorly in the duodenal bulb.

Vomiting-related UGIB

During vomiting, the lower esophagus and upper stomach are forcibly inverted. Vomiting attributable to any cause can lead to a mucosal tear of the lower esophagus or upper stomach. The depth of the tear determines the severity of the bleeding. Rarely, vomiting can result in esophageal rupture (Boerhaave syndrome), leading to bleeding, mediastinal air entry, left pleural effusion (salivary amylase can be present) or left pulmonary infiltrate, and subcutaneous emphysema.

Mallory-Weiss tears in UGIB

Mallory-Weiss tears account for 15% of acute upper GI hemorrhage.[10] Kenneth Mallory and Soma Weiss first described the syndrome in 1929.[18] The massive UGIB results from a tear in the mucosa of the gastric cardia.

This linear mucosal laceration is the result of forceful vomiting, retching, coughing, or straining. These actions create a rapid increase in the gradient between intragastric and intrathoracic pressures, leading to a gastric mucosal tear from the forceful distention of the gastroesophageal junction.[19] In 80-90% of cases, this is a single, 1.75- to 2.5-cm mucosal tear along the lesser curve of the stomach just distal to the gastroesophageal junction.[18]

Go to Mallory-Weiss Tear for complete information on this topic.

Acute stress gastritis in UGIB

Acute stress gastritis results from predisposing clinical conditions that have the potential to alter the local mucosal protective barriers, such as mucus, bicarbonate, blood flow, and prostaglandin synthesis. Any disease process that disrupts the balance of these factors results in diffuse gastric mucosal erosions.

This is most commonly observed in patients who have undergone episodes of shock, multiple trauma, acute respiratory distress syndrome, systemic respiratory distress syndrome, acute renal failure, and sepsis.

The principal mechanisms involved are decreased splanchnic mucosal blood flow and altered gastric luminal acidity.

Dieulafoy lesions in UGIB

The Dieulafoy lesion, first described in 1896, is a vascular malformation of the proximal stomach, usually within 6 cm of the gastroesophageal junction along the lesser curvature of the stomach. However, it can occur anywhere along the GI tract. This lesion accounts for 2-5% of acute UGIB episodes.[20]

Endoscopically, the lesion appears as a large submucosal vessel that has become ulcerated. Because of the large size of the vessel, bleeding can be massive and brisk. The vessel rupture usually occurs in the setting of chronic gastritis, which may induce necrosis of the vessel wall. Alcohol consumption is reportedly associated with the Dieulafoy lesion.

In a review of 149 cases, the Dieulafoy lesion mostly occurred in men and mostly in those in their third to tenth decade.[21]

NSAIDs in UGIB

NSAIDs cause gastric and duodenal ulcers by inhibiting cyclooxygenase, which causes decreased mucosal prostaglandin synthesis and results in impaired mucosal defenses. Daily NSAID use causes an estimated 40-fold increase in gastric ulcer creation and an 8-fold increase in duodenal ulcer creation.[16]

Long-term NSAID use is associated with a 20% incidence in the development of mucosal ulceration.[22] Medical therapy includes avoiding the ulcerogenic drug and beginning a histamine-2 (H2)–receptor antagonist or a proton pump inhibitor that provides mucosal protection.

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Epidemiology

Annually, approximately 100,000 patients are admitted to US hospitals for therapy for UGIB. In the United Kingdom, UGIB accounts for 70,000 hospital admissions each year, with the majority of cases nonvariceal in origin.[23]

UGIB is a common occurrence throughout the world. In France, a report concludes that the mortality from UGIB has decreased from about 11% to 7%; however, a similar report from Greece finds no decrease in mortality. In a nationwide study from Spain, UGIB was 6 times more common than lower GI bleeding.[24]

The incidence of UGIB is 2-fold greater in males than in females, in all age groups; however, the death rate is similar in both sexes.[9]

The population with UGIB has become progressively older, with a concurrent increase in significant comorbidities that increase mortality. Mortality increases with older age (>60 y), in both males and females.[22]

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Prognosis

As previously mentioned, age older than 60 years is an independent marker for a poor outcome in upper gastrointestinal bleeding (UGIB),[25] with the mortality rate ranging from 12-25% in this group of patients.

The American Society for Gastrointestinal Endoscopy (ASGE) grouped patients with UGIB according to age and correlated age category to the risk of mortality. The ASGE found a mortality rate of 3.3% for patients aged 21-31 years, a rate of 10.1% for those aged 41-50 years, and a rate of 14.4% for those aged 71-80 years.[25]

The following risk factors are associated with an increased mortality, recurrent bleeding, the need for endoscopic hemostasis, or surgery[14, 26] :

  • Age older than 60 years
  • Severe comorbidity
  • Active bleeding (eg, witnessed hematemesis, red blood per nasogastric tube, fresh blood per rectum)
  • Hypotension
  • Red blood cell transfusion greater than or equal to 6 units
  • Inpatient at time of bleed
  • Severe coagulopathy

Patients who present in hemorrhagic shock have a mortality rate of up to 30%.

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Contributor Information and Disclosures
Author

Maurice A Cerulli, MD, FACP, FACG, FASGE, AGAF Associate Professor of Clinical Medicine, Albert Einstein College of Medicine of Yeshiva University; Associate Professor of Clinical Medicine, Hofstra Medical School

Maurice A Cerulli, MD, FACP, FACG, FASGE, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, New York Society for Gastrointestinal Endoscopy, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Coauthor(s)

Shahzad Iqbal, MD Advanced Endoscopy Fellow, Department of Gastroenterology, Columbia University Medical Center

Shahzad Iqbal, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Acknowledgements

James de Caestecker, DO Instructor, Department of Surgery, MCP Hahnemann University

James de Caestecker, DO is a member of the following medical societies: American College of Surgeons

Disclosure: Nothing to disclose.

Michael A Grosso, MD Consulting Staff, Department of Cardiothoracic Surgery, St Francis Hospital

Michael A Grosso, MD is a member of the following medical societies: American College of Surgeons, Society of Thoracic Surgeons, and Society of University Surgeons

Disclosure: Nothing to disclose.

Douglas M Heuman, MD, FACP, FACG, AGAF Chief of Hepatology, Hunter Holmes McGuire Department of Veterans Affairs Medical Center; Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine

Douglas M Heuman, MD, FACP, FACG, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, and American Gastroenterological Association

Disclosure: Novartis Grant/research funds Other; Bayer Grant/research funds Other; Otsuka Grant/research funds None; Bristol Myers Squibb Grant/research funds Other; Scynexis None None; Salix Grant/research funds Other; MannKind Other

Alex Jacocks, MD Program Director, Professor, Department of Surgery, University of Oklahoma School of Medicine

Disclosure: Nothing to disclose.

Jason Straus, MD Staff Physician, Department of Surgery, Wright State University School of Medicine

Jason Straus, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, and Society of American Gastrointestinal and Endoscopic Surgeons

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Ulcer with active bleeding.
Ulcer with a clean base.
Diagram of an ulcer with a clean base.
Ulcer with an overlying clot.
Ulcer with a visible vessel.
Diagram of an ulcer with a visible vessel.
Table 1. Probable Source of GI Bleeding Within the Gut
Clinical Indicator Probability of Upper GI Source Probability of Lower GI Source
Hematemesis Almost certain Rare
Melena Probable Possible
Hematochezia Possible Probable
Blood-streaked stool Rare Almost certain
Occult blood in stool Possible Possible
Table 2. Estimated Fluid and Blood Losses in Shock
  Class 1 Class 2 Class 3 Class 4
Blood Loss, mL Up to 750 750-1500 1500-2000 >2000
Blood Loss,% blood volume Up to 15% 15-30% 30-40% >40%
Pulse Rate, bpm < 100 >100 >120 >140
Blood Pressure Normal Normal Decreased Decreased
Respiratory Rate Normal or Increased Decreased Decreased Decreased
Urine Output, mL/h >35 30-40 20-30 14-20
CNS/Mental Status Slightly



anxious



Mildly



anxious



Anxious,



confused



Confused,



lethargic



Fluid Replacement, 3-for-1 rule Crystalloid Crystalloid Crystalloid and blood Crystalloid and blood
Table 3. Effect of Number of Packed Erythrocyte Transfusions on Need for Surgery and Mortality from UGIB
Number of Units Transfused Need for Surgery, % Mortality Rate, %
0 4 4
1-3 6 14
4-5 17 28
>5 57 43
Table 4. Effect of the Color of the Nasogastric Aspirate and of the Stool on UGIB Mortality Rate
Nasogastric Aspirate Color Stool Color Mortality Rate, %
Clear Brown or red 6
Coffee-ground Brown or black 8.2
  Red 19.1
Red blood Black 12.3
  Brown 19.4
  Red 28.7
Table 5. Ulcer Characteristics and Correlations
Ulcer Characteristics Prevalence Rate, % Rebleeding Rate, % Surgery Rate, % Mortality Rate, %
Clean base 42 5 0.5 2
Flat spot 20 10 6 3
Adherent clot 17 22 10 7
Visible vessel 17 43 34 11
Active bleeding 18 55 35 11
Table 6. Recurrent Ulcer and Postgastrectomy Syndromes After Operations for Duodenal Ulcer
Original Operation Recurrence Rate, % Postgastrectomy Syndrome Rate, % Mortality Rate, %
Proximal gastric vagotomy 10 5 0.1
Truncal vagotomy and drainage 7 20-30 < 1
Truncal vagotomy and antrectomy



Billroth I or Billroth II



1 30-50 0-5
Truncal vagotomy and antrectomy



Roux-en-Y



5-10 50-60 0-5
Table 7. Effects of Operations for PUD on Gastric Emptying and Motility
Operation Antral Innervation Liquid Emptying Solid Emptying
Proximal gastric vagotomy Preserved Fast Normal
Truncal vagotomy Divided Fast Slow
Truncal vagotomy and drainage Divided Fast Fast
Truncal vagotomy and antrectomy Divided Fast Fast
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